Recent advances and research in management of Diabetes with traditionally used natural therapies have resulted in development of products from that facilitate production and proper utilization of insulin in the body. These preparations (Biogetica) are natural and work in conjugation with conventional therapies as supportive treatment protocols, they are absolutely safe and the patients are never at risk of developing hypoglycemic attacks due to the therapies.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Exenatide (Byetta) was the first drug of the GLP-1 agonist group. It originated from an interesting source, the saliva of the Gila monster. Scientists observed that this small lizard could go a long time without eating. They discovered a substance in its saliva that slowed stomach emptying, thus making the lizard feel fuller for a longer time. This substance resembled the hormone GLP-1.
Formal recommendations on how to reverse type 2 diabetes in clinical practice must await further studies. In the meantime, it will be helpful for all individuals with newly diagnosed type 2 diabetes to know that they have a metabolic syndrome that is reversible. They should know that if it is not reversed, the consequences for future health and cost of life insurance are dire, although these serious adverse effects must be balanced against the difficulties and privations associated with a substantial and sustained change in eating patterns. For many people, this may prove to be too high a price to pay, but for those who are strongly motivated to escape from type 2 diabetes, the new understanding gives clear direction. Physicians need to accept that long-term weight loss is achievable for a worthwhile proportion of patients (96). In the United States, diabetes costs $174 billion annually (97), and in the United Kingdom, it accounts for 10% of National Health Service expenditure. Even if only a small proportion of patients with type 2 diabetes return to normal glucose control, the savings in disease burden and economic cost will be enormous.
Chinese medicine has been using cinnamon for medicinal purposes for hundreds of years. It has been the subject of numerous studies to determine its effect on blood glucose levels. A 2011 study has shown that cinnamon, in whole form or extract, helps lower fasting blood glucose levels. More studies are being done, but cinnamon is showing promise for helping to treat diabetes.
Dr. Mona Morstein is a naturopathic physician with a medical practice focused in integrative diabetes treatment. Her clinic, Arizona Integrative Medical Solutions, is located in Tempe, Arizona, where she sees patients of all ages and genders for acute and chronic conditions. An expert on prediabetes and diabetes, she is a frequent lecturer at conferences and webinars, and is the founder and executive director of The Low Carb Diabetes Association. Dr. Morstein is also a member of the Arizona Diabetes Coalition. Visit her website lowcarbdiabetes.org
The problem, of course, has not been solved – the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take metformin to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of metformin cannot force any more sugar into the body.
Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
Regular blood testing, especially in type 1 diabetics, is helpful to keep adequate control of glucose levels and to reduce the chance of long term side effects of the disease. There are many (at least 20+) different types of blood monitoring devices available on the market today; not every meter suits all patients and it is a specific matter of choice for the patient, in consultation with a physician or other experienced professional, to find a meter that they personally find comfortable to use. The principle of the devices is virtually the same: a small blood sample is collected and measured. In one type of meter, the electrochemical, a small blood sample is produced by the patient using a lancet (a sterile pointed needle). The blood droplet is usually collected at the bottom of a test strip, while the other end is inserted in the glucose meter. This test strip contains various chemicals so that when the blood is applied, a small electrical charge is created between two contacts. This charge will vary depending on the glucose levels within the blood. In older glucose meters, the drop of blood is placed on top of a strip. A chemical reaction occurs and the strip changes color. The meter then measures the color of the strip optically.
Esophageal cancer is a disease in which malignant cells form in the esophagus. Risk factors of cancer of the esophagus include smoking, heavy alcohol use, Barrett's esophagus, being male and being over age 60. Severe weight loss, vomiting, hoarseness, coughing up blood, painful swallowing, and pain in the throat or back are symptoms. Treatment depends upon the size, location and staging of the cancer and the health of the patient.
Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.
The big news with the use of fig leaves is that they have anti-diabetic properties. The diabetic needs less insulin when on a treatment of using the fig leaf extract. The diabetic should take the extract with breakfast, first thing in the morning. An additional remedy is to boil the leaves of the fig in some freshly filtered waster and drink this as a tea. Read the whole article on fig leaves and diabetes:
For type 2 diabetics, diabetic management consists of a combination of diet, exercise, and weight loss, in any achievable combination depending on the patient. Obesity is very common in type 2 diabetes and contributes greatly to insulin resistance. Weight reduction and exercise improve tissue sensitivity to insulin and allow its proper use by target tissues. Patients who have poor diabetic control after lifestyle modifications are typically placed on oral hypoglycemics. Some Type 2 diabetics eventually fail to respond to these and must proceed to insulin therapy. A study conducted in 2008 found that increasingly complex and costly diabetes treatments are being applied to an increasing population with type 2 diabetes. Data from 1994 to 2007 was analyzed and it was found that the mean number of diabetes medications per treated patient increased from 1.14 in 1994 to 1.63 in 2007.
Cinnamon contains a bioactive compound that can help to fight and prevent diabetes. Cinnamon is known to stimulate the insulin activity and thus regulate the blood sugar level. As excess of anything is bad, likewise cinnamon if taken in excess can increase the risk of liver damage due to a compound called coumarin present in it. The true cinnamon, not the one buy from shops (Cassia cinnamon) is safer to have.
But look closer. The results may be statistically significant, but they’re not that impressive compared to medication. Cinnamon lowered A1C by 0.09%, versus the usual 1% with medication. Give A1c reflects overall glucose trends, cinnamon doesn’t look that impressive. Even at the extreme of the confidence interval, cinnamon has, at best, 10% of the efficacy of drug treatments. At worst, it’s completely ineffective.